Could mitochondrial dysfunction be a marker to distinguish FM from ME/CFS?

Editor's comment: Mitochondria are the energy producers of the cells. The mitochondria supply this energy in the form of adenosine triphosphate (ATP), the molecule upon which all cellular functions in the body depend. Coenzyme Q10 acts as the catalyst that makes it possible for the mitochondria to produce ATP. Previous research has demonstrated that mitochondrial dysfunction is present in both fibromyalgia and ME/CFS (chronic fatigue syndrome). However, this is the first study to suggest that the type of mitochondrial dysfunction may serve as a marker that is able to differentiate FM from ME/CFS. For more information about mitochondrial dysfunction in FM, see “Dr. Myhill on Fibromyalgia and Mitochondrial Dysfunction.”

Could mitochondrial dysfunction be a differentiating marker between Chronic Fatigue Syndrome and Fibromyalgia?

By J. Castro-Marrero, et al.

Abstract:

Chronic Fatigue Syndrome (CFS) and Fibromyalgia (FM) are complex and serious illnesses. It is estimated to affects up to 2.5% and 5% of the general population worldwide, respectively. The aetiology is unknown; however, recent studies suggest that mitochondrial dysfunction has been involved in the pathophysiology of both conditions.

We have investigated the possible association between mitochondrial biogenesis and oxidative stress in patients with CFS and FM. We studied 23 CFS patients, 20 FM patients and 15 healthy controls.

On the contrary, CFS/FM patients had significantly increased levels of lipid peroxidation, respectively (p<0.001 for both CFS and FM patients respect to controls) indicative of oxidative stress-induced damage.

Mitochondrial citrate synthase activity was significantly lower in FM patients (p<0.001) and however, in CFS resulted in similar levels than controls.

Expression levels of PGC-1? and TFAM by immunoblotting showed significantly lower in FM patients (p<0.001) and were normal in CFS subjects compared to healthy controls.

These data lead to the hypothesis that mitochondrial dysfunction-dependent events could be a marker of differentiation between CFS and FM indicating the mitochondria as a new potential therapeutic target for these conditions.

but I wonder how they separated FM from ME/CFS patients. In practice this is not easy to do.

Around 50% of people with ME/CFS fit the criteria for FM and vice versa. so what do they have? Both illnesses. I know some people can have "ME/CFS" without much widespread pain and you can have some people with FM and not post-exertional malaise.

To complicate matters you can have people with ME/CFS with more pain than fatigue and you can have some people who fit the criteria for ME/CFS but have little post-exertional malaise.

There is so much clarification needed within these disorders. To distinguish them on the basis of mitochondrial dysfunction is unlikely until the diagnostics are clearer. I suspect the authors small numbers of subjects were a similar subgroup.

What i understand from the papers, is that the mitochondra dysfunction is different in fibro compared to cfs. In fibro cells its not withstanding burning oxygen and switches to sugar for energy which causes a build up in lactic acid causes tight muscles pain and spasm and tisdue damage. Where as cfs its to do with the way it processes sugar, affecting energy and hormones. Interesting.